External load influences internal load in resistance training (RT). The purpose of the present study was to compare the total volume-load, perceptual and stress responses during three different RT protocols. Twelve resistance-trained men completed three different RT protocols with the back squat and bench press exercises: (1) power (POW) (5 sets of 6 repetitions at 50%1RM, 2-min of rest), (2) hypertrophy (HYP) (5 sets-to-failure at 75%1RM, 2-min of rest), and (3) strength (STR) (5 sets-to-failure at 90%1RM, 3-min of rest). Volume-load (kg × reps.), session rating of perceived exertion (sRPE), training impulse (TRIMP; reps. × sRPE), cortisol, immunoglobulin A (IgA), lactate, and creatine kinase (CK) were assessed before and/or after the sessions. HYP was the most demanding session in terms of volume-load (p < 0.001), TRIMP (p < 0.001), cortisol (p = 0.001), lactate (p < 0.001), and CK (p = 0.001). Despite POW exhibited a greater volume-load than STR (p = 0.016), the latter exhibiting a greater sRPE (p < 0.001), and a greater post-session CK (p = 0.05). However, the TRIMP of STR and POW were not statistically different (152 vs. 260 AU; p = 0.089). These specific responses could be meditated by the presence of muscular failure. When pooling all the sessions, significant correlations were revealed among external and internal stress markers (r = 0.35-0.80; p ≤ 0.05). The use of TRIMP could be recommended as a simple and valid monitoring tool which integrates into a single parameter the internal and the external loads of RT sessions.
- MeSH
- Analysis of Variance MeSH
- Biomarkers blood MeSH
- Adult MeSH
- Hydrocortisone blood MeSH
- Hypertrophy MeSH
- Immunoglobulin A blood MeSH
- Creatine Kinase blood MeSH
- Lactic Acid blood MeSH
- Humans MeSH
- Young Adult MeSH
- Resistance Training methods MeSH
- Muscle Strength physiology MeSH
- Physical Exertion physiology MeSH
- Muscle Development physiology MeSH
- Weight Lifting physiology MeSH
- Check Tag
- Adult MeSH
- Humans MeSH
- Young Adult MeSH
- Male MeSH
- Publication type
- Journal Article MeSH
Typically, mammalian and avian models have been used to examine the effects of ammonia on skeletal muscle. Hyperammonemia causes sarcopenia or muscle wasting, in mammals and has been linked to sarcopenia in liver disease patients. Avian models of skeletal muscle have responded positively to hyperammonemia, differing from the mammalian response. Fish skeletal muscle has not been examined as extensively as mammalian and avian muscle. Fish skeletal muscle shares similarities with avian and mammalian muscle but has notable differences in growth, fiber distribution, and response to the environment. The wide array of body sizes and locomotion needs of fish also leads to greater diversity in muscle fiber distribution and growth between different fish species. The response of fish muscle to high levels of ammonia is important for aquaculture and quality food production but has not been extensively studied to date. Understanding the differences between fish, mammalian and avian species' myogenic response to hyperammonemia could lead to new therapies for muscle wasting due to a greater understanding of the mechanisms behind skeletal muscle regulation and how ammonia effects these mechanisms. This paper provides an overview of fish skeletal muscle and ammonia excretion and toxicity in fish, as well as a comparison to avian and mammalian species.
- MeSH
- Ammonia pharmacology toxicity MeSH
- Hyperammonemia etiology MeSH
- Liver Cirrhosis etiology MeSH
- Muscle Fibers, Skeletal drug effects MeSH
- Muscle, Skeletal drug effects metabolism MeSH
- Birds MeSH
- Fishes MeSH
- Sarcopenia etiology MeSH
- Mammals MeSH
- Muscular Atrophy metabolism physiopathology MeSH
- Muscle Development drug effects physiology MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH
- Review MeSH
The biochemical properties of muscle extracellular matrix are essential for stem cell adhesion, motility, proliferation and myogenic development. Recombinant elastin-like polypeptides are synthetic polypeptides that, besides maintaining some properties of the native protein, can be tailored by fusing bioactive sequences to their C-terminal. Our laboratory synthesized several Human Elastin-Like Polypeptides (HELP) derived from the sequence of human tropoelastin. Here, we developed a novel HELP family member by fusing the elastin-like backbone to the sequence of human Epidermal Growth Factor. We employed this synthetic protein, named HEGF, either alone or in combination with other proteins of the HELP family carrying RGD-integrin binding sites, as adhesion substrate for C2C12 myoblasts and satellite cells primary cultures. Adhesion of myoblasts to HEGF-based substrates induced scattering, decreased adhesion and cytoskeleton assembly; the concomitant presence of the RGD motifs potentiated all these effects. Recombinant substrates induced myoblasts proliferation, differentiation and the development of multinucleated myotubes, thus favoring myoblasts expansion and preserving their myogenic potential. The effects induced by adhesion substrates were inhibited by AG82 (Tyrphostin 25) and herbimycin A, indicating their dependence on the activation of both the EGF receptor and the tyrosine kinase c-src. Finally, HEGF increased the number of muscle stem cells (satellite cells) derived from isolated muscle fibers in culture, thus highlighting its potential as a novel substrate for skeletal muscle regeneration strategies.
- MeSH
- Cell Adhesion physiology MeSH
- Cell Differentiation physiology MeSH
- Epidermal Growth Factor metabolism physiology MeSH
- Extracellular Matrix MeSH
- Stem Cells cytology MeSH
- Muscle Fibers, Skeletal cytology MeSH
- Muscle, Skeletal cytology MeSH
- Cells, Cultured MeSH
- Myoblasts cytology MeSH
- Mice, Inbred C57BL MeSH
- Mice MeSH
- Cell Movement physiology MeSH
- Primary Cell Culture MeSH
- Cell Proliferation physiology MeSH
- Satellite Cells, Skeletal Muscle metabolism physiology MeSH
- Signal Transduction MeSH
- Muscle Development physiology MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
One of the greatest enigmas of modern biology is how the geometry of muscular and skeletal structures are created and how their development is controlled during growth and regeneration. Scaling and shaping of vertebrate muscles and skeletal elements has always been enigmatic and required an advanced technical level in order to analyse the cell distribution in 3D. In this work, synchrotron X-ray computed microtomography (µCT) and chemical contrasting has been exploited for a quantitative analysis of the 3D-cell distribution in tissues of a developing salamander (Pleurodeles waltl) limb - a key model organism for vertebrate regeneration studies. We mapped the limb muscles, their size and shape as well as the number and density of cells within the extracellular matrix of the developing cartilage. By using tomographic approach, we explored the polarity of the cells in 3D, in relation to the structure of developing joints. We found that the polarity of chondrocytes correlates with the planes in joint surfaces and also changes along the length of the cartilaginous elements. Our approach generates data for the precise computer simulations of muscle-skeletal regeneration using cell dynamics models, which is necessary for the understanding how anisotropic growth results in the precise shapes of skeletal structures.
The bulbocavernosus (BC) is a sexually dimorphic muscle observed only in males. Androgen receptor knockout mouse studies show the loss of BC formation. This suggests that androgen signaling plays a vital role in its development. Androgen has been known to induce muscle hypertrophy through satellite cell activation and myonuclei accretion during muscle regeneration and growth. Whether the same mechanism is present during embryonic development is not yet elucidated. To identify the mechanism of sexual dimorphism during BC development, the timing of morphological differences was first established. It was revealed that the BC was morphologically different between male and female mice at embryonic day (E) 16.5. Differences in the myogenic process were detected at E15.5. The male BC possesses a higher number of proliferating undifferentiated myoblasts. To identify the role of androgen signaling in this process, muscle-specific androgen receptor (AR) mutation was introduced, which resulted in no observable phenotypes. Hence, the expression of AR in the BC was examined and found that the AR did not colocalize with any muscle markers such as Myogenic differentiation 1, Myogenin, and paired box transcription factor 7. It was revealed that the mesenchyme surrounding the BC expressed AR and the BC started to express AR at E15.5. AR mutation on the nonmyocytic cells using spalt-like transcription factor 1 (Sall1) Cre driver mouse was performed, which resulted in defective BC formation. It was revealed that the number of proliferating undifferentiated myoblasts was reduced in the Sall1 Cre:AR(L-/Y) mutant embryos, and the adult mutants were devoid of BC. The transition of myoblasts from proliferation to differentiation is mediated by cyclin-dependent kinase inhibitors. An increased expression of p21 was observed in the BC myoblast of the Sall1 Cre:AR(L-/Y) mutant and wild-type female. Altogether this study suggests that the nonmyocytic AR may paracrinely regulate the proliferation of myoblast possibly through inhibiting p21 expression in myoblasts of the BC.
- MeSH
- Receptors, Androgen genetics metabolism MeSH
- Time Factors MeSH
- Embryo, Mammalian embryology metabolism MeSH
- Immunohistochemistry MeSH
- Cyclin-Dependent Kinase Inhibitor p21 metabolism MeSH
- Microscopy, Electron, Scanning MeSH
- Mutation MeSH
- Myoblasts cytology metabolism MeSH
- Mice, Inbred ICR MeSH
- Mice, Knockout MeSH
- Mice, Transgenic MeSH
- Mice MeSH
- Perineum embryology MeSH
- Cell Proliferation MeSH
- Sex Factors MeSH
- Muscles embryology metabolism ultrastructure MeSH
- Pregnancy MeSH
- Transcription Factors genetics metabolism MeSH
- Muscle Development genetics physiology MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Mice MeSH
- Pregnancy MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Research Support, N.I.H., Extramural MeSH
Many stress conditions are accompanied by skeletal muscle dysfunction and regeneration, which is essentially a recapitulation of the embryonic development. However, regeneration usually occurs under conditions of hypothalamus-pituitary-adrenal gland axis activation and therefore increased glucocorticoid (GC) levels. Glucocorticoid receptor (GR), the main determinant of cellular responsiveness to GCs, exists in two isoforms (GRalpha and GRbeta) in humans. While the role of GRalpha is well characterized, GRbeta remains an elusive player in GC signalling. To elucidate basic characteristics of GC signalling in the regenerating human skeletal muscle we assessed GRalpha and GRbeta expression pattern in cultured human myoblasts and myotubes and their response to 24-hour dexamethasone (DEX) treatment. There was no difference in GRalpha mRNA and protein expression or DEX-mediated GRalpha down-regulation in myoblasts and myotubes. GRbeta mRNA level was very low in myoblasts and remained unaffected by differentiation and/or DEX. GRbeta protein could not be detected. These results indicate that response to GCs is established very early during human skeletal muscle regeneration and that it remains practically unchanged before innervation is established. Very low GRbeta mRNA expression and inability to detect GRbeta protein suggests that GRbeta is not a major player in the early stages of human skeletal muscle regeneration.
- MeSH
- Cell Culture Techniques methods MeSH
- Dexamethasone therapeutic use MeSH
- Gene Expression genetics MeSH
- Financing, Organized MeSH
- Glucocorticoids genetics metabolism MeSH
- Real-Time Polymerase Chain Reaction utilization MeSH
- Humans MeSH
- Musculoskeletal System physiopathology MeSH
- Myoblasts, Skeletal physiology pathology drug effects MeSH
- Stress, Psychological metabolism physiopathology pathology MeSH
- Receptors, Glucocorticoid genetics metabolism MeSH
- Statistics as Topic MeSH
- Muscle Development physiology genetics drug effects MeSH
- Blotting, Western utilization MeSH
- Check Tag
- Humans MeSH
- MeSH
- Rats MeSH
- Motor Neurons physiology MeSH
- Carrier Proteins analysis physiology MeSH
- Muscle Development physiology MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Animals MeSH
- Publication type
- Congress MeSH
- MeSH
- Anthropometry methods MeSH
- Biomedical Research * methods organization & administration MeSH
- Humans MeSH
- Longitudinal Studies MeSH
- Adolescent MeSH
- Sex Distribution MeSH
- Statistics as Topic MeSH
- Muscle Strength * physiology MeSH
- Sports Medicine methods MeSH
- Age Factors MeSH
- Muscle Development * physiology MeSH
- Check Tag
- Humans MeSH
- Adolescent MeSH
- Male MeSH
- Female MeSH
